The experiments proposed here will be carried out as part of a general investigation into the neural mechanisms underlying ethanol's disruptive effect on higher-order sensory functions. In particular, selective processing of sensory information in the presence of distraction is known to be a parameter of human performance which is markedly disturbed during intoxication. The PI has developed and utilized a relatively simple neurophysiological system for studying selective sensory processing in the cerebral cortex and is currently using this model in assessments of the effects of acute ethanol intoxication. This model involves recording single units in the primary somatosensory (SI) cortex of rats. Computer techniques are used to measure two types of behavior related sensory modulation: 1) sensory facilitation in "immobile arousal" behaviors, and 2) inhibitory gating of cutaneous sensory transmission from the forepaw to these cells during, and in correlation with, limb movements. These inhibitory controls only allow this sensory information to reach certain cortical cells during precise phases of the step cycle. Ethanol, among its other effects, appears to reduce or abolish the sensory facilitations seen in arousal, and also the inhibitory controls seen in movement. These occur in a dose-dependent fashion. Thus, even low ethanol doses appear to severely compromise the brain's control of its own sensory input. The experiments proposed here will: 1) investigate these findings in the SI cortex more thoroughly, 2) utilize the "Preferring" and "Non-preferring" rat strains (of Li, Lumeng, et al.) in similar experiments, 3) investigate the possibility that ethanol's reduction of inhibitory gating controls may result from disruption of activity in the adjacent motor cortex (one possible source of the gating bias signal), and 4) develop an operantly controlled behavioral paradigm for "passive" selective attention in which a sensory stimulus is made "significant" by pairing it with a reward.